Why the study?
Does intravenous pentolinium alter cardiovascular hemodynamics and reflex responses in anesthetized dogs?
Does intravenous pentolinium alter cardiovascular hemodynamics and reflex responses in anesthetized dogs?
Intravenous pentolinium in anesthetized dogs blocks the cardiac vagus and sympathetic nervous system, altering pulse rate, blood pressure, and cardiac output while blunting reflex cardiovascular responses.
Should not guide clinical autonomic blockade; leaves open translational hemodynamic research in humans.
Pentolinium (5 mgm./kgm.) injected intravenously into dogs anesthetized with pentobarbital caused the pulse rate to approach that of dogs with surgical cardiac denervation. The higher the initial pulse rate, the greater the decrease after the drug; rates under 100/min. were increased. Changes in arterial pressure followed a similar pattern, and the changes in both systemic and pulmonary arterial pressures were correlated with the changes in pulse rate. The cardiac output was decreased. Pressor responses to injected adrenaline and noradrenaline were greater after pentolinium. Total peripheral resistance, respiratory rate, respiratory minute volume, and oxygen consumption were not changed significantly, but local (hind-leg) resistance was decreased in two of three experiments. Pentolinium abolished or reduced markedly the cardiovascular responses to reduced carotid sinus pressure, tilting, acute hypoxia, large doses of acetylcholine, and hemorrhage. The cardiac vagus and the cardiovascular part of the sympathetic nervous system are blocked, but the experiments suggest that the adrenal medulla may not be completely blocked by 5 mgm./kgm. pentolinium.
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Spoerel et al. (1956) studied this question.
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